The synthesis of prostaglandins occurs in the eye. Aspirin-like compounds inhibit prostaglandin synthesis. Arachidonic acid, a precursor of PGE, elevates intraocular pressure and aqueous humor protein when applied topically. Aspirin-like compounds prevent the elevation of intraocular pressure and aqueous protein induced by arachidonic acid. Many ocular inflammatory responses may be mediated by prostaglandins. Thus, inhibition of prostaglandin synthesis or action may be effective in the treatment of a variety of ocular conditions and obviate the toxic side effects of corticosteroids. The present proposal will continue to study the effect of many inhibitors of prostaglandin action and its synthesis, on the intraocular pressure and aqueous humor protein elevations induced by arachidonic acid in rabbits and monkeys. It will investigate the specificity of these blockers by testing their effects on non-prostaglandin mediated stimuli such as nitrogen mustard. The effects of the most potent compounds will be examined on experimental uveitis produced by intravitreal injections of bovine serum albumin. Hopefully, clinical therapeutic agents will be identified. In addition the mechanism and inhibition of carboxylic ionophoreinduced elevation of intraocular pressure will be investigated, as well as the interactions of these calcium ion carriers with catecholamines. Measurements of cyclic AMP, calcium, and ascorbate in aqueous humor will be employed.